The document discusses Inflammatory Bowel Disease (IBD), including Ulcerative Colitis and Crohn's Disease, providing details on their etiology, clinical manifestations, investigations, medical and surgical management, and cancer risk. IBD is characterized by idiopathic intestinal inflammation that has genetic and environmental risk factors and can involve any part of the gastrointestinal tract. Management involves a multidisciplinary approach including medications, nutrition, and surgery.

1. INFLAMMATORY
BOWEL DISEASE
BY DR K.NAGA SANTOSH
ASSISTANT PROFESSOR
DEPARTMENT OF GENERAL SURGERY
GUNTUR MEDICAL COLLEGE

2. • IBD is charecterised by presence of idiopathic intestinal inflammation.
• IBD includes 1.Chrons disease 2.Ulcerative colitis 3.Indeterminate Colitis.
The incidence and prevalence of IBD is highest in Europe and North
America 3 in 1000 people. The overall incidence is steadily rising
worldwide, linked to improved public hygiene, dietary changes and
industrialisation.
• Both UC and CD occur in individuals who may have a genetic
predisposition and who are exposed to environmental factors that
trigger abnormal immune responses that lead to intestinal
infammation.
• Microscopic colitis includes two main subtypes: lymphocytic colitis
and collagenous colitis (CC).
• The aetiology is uncertain but may refect inappropriate immune
responses to alterations in the gut microenvironment consequent to

3. ULCERATIVE COLITIS
• Mucosal inflammation
• Usually confined to large intestine, RECTUM is always involved with varying involvement of
proximal colon.
• If associated with pancolitis, secondary inflammation in terminal ileum can be seen known
as BACKWASH ILEITIS.
• Ulcerative colitis is chronic condition with episodes of relapse and remission,
• Early relapse and persistent disease in 1st 2years of life is indicative of severe disease.
• HPE findings: 1.Atrophy and distortion of crypts
• 2.Irregularity of mucosal villi
• 3.Basal plasmocytosis
• 4.Mucus depletion
• Presence of stricture or irregular mucosal swelling (DALM) is suspicios is coexisting
carcinoma.

4. CROHNS DISEASE
• Discontinuous trans mural inflammation can involve any part of GIT
from mouth to anus
• Most typically involves Distal Ileum , large bowel and anus.
• Rectal sparing is seen when colon is involved
• HPE Findings
• 1.skip lesions
• 2.involvement of terminal ileum and presence of granulomas
• 3.Marked inflammation of proximal colon
• 4.Stricture.

5. INDETERMINATE COLITIS
•When endoscopic and histological appearances do
not categorically confrm either UC or CD, and the
term IC is used, the clinical phenotype may help
defne the diagnosis, especially if there are features
of small bowel or perianal disease suggestive of CD.
•Patients with IC may later come to a definitive
diagnosis of UC or CD, depending on the disease
course.

7. CLINICAL FEATURES
• The clinical manifestations of IBD primarily depend on the diagnosis (either CD or UC),
the location (small or large intestine, or both) and the extent of the disease.
• In the large bowel, the clinical presentation depends in large part on the extent of
disease. If infammation is confned to the rectum (proctitis), no systemic upset and
extra-alimentary manifestations are rare. The main symptoms are rectal bleeding,
tenesmus and mucous discharge.
• The disease often remains confined to the rectum, usually with a benign course.
• Colitis is almost always associated with bloody diarrhoea and urgency.
• Severe and/or extensive colitis may result in anaemia, hypoproteinaemia and
electrolyte disturbances. Pain is unusual. Children with poorly controlled colitis may
have impaired growth.
• The more extensive the disease, the more likely extraintestinal manifestations are to
occur.
• Extensive colitis is also associated with systemic illness, characterised by malaise, loss

8. TRUELOVEANDWITTS SEVERITY CLASSIFICATION OF COLITIS
Is determined by the frequency of bowel action and the presence of systemic signs of illness
Mild disease is characterised by1. fewer than four stools daily, with or without bleeding.
2. no systemic signs of toxicity.
Moderate disease corresponds to1. more than four stools daily,
2. with few signs of systemic illness like anemia and abdominal pain
3.Infammatory markers like ESR and CRP are often raised.
Severe disease corresponds to 1.more than six bloody stools a day and
2.evidence of systemic illness, with fever, tachycardia, anaemia and
3.raised infammatory markers.
4.Hypoalbuminaemia is common and an ominous fnding.

9. • Fulminant disease is associated with
• 1.more than 10 bowel movements daily,
• 2.fever, tachycardia, continuous bleeding, anaemia,
hypoalbuminaemia, abdominal tenderness and distension,
• 3.the need for blood transfusion and, in the most severe cases,
progressive colonic dilation (toxic megacolon). This is a very
signifcant fnding, suggestive of disintegrative colitis, and an
indication for emergency surgery if colonic perforation is to be
avoided.

10. ACUTE COLITISWITHTOXIC MEGACOLON

11. EXTRA INTESTINAL MANIFESTATIONS
• Arthritis occurs in around 15% of patients and is typically an
asymmetrical large joint polyarthropathy, afecting knees,
ankles, elbows and wrists.
• Sacroiliitis and ankylosing spondylitis are 20 times more
common in patients with UC than in the general population and are
associated with the HLA-B27 genotype.
• Sclerosing cholangitis is associated with UC and can progress to
cirrhosis and hepatocellular failure. Cholangiocarcinoma is a rare
association, but its frequency is not infuenced by colectomy).
• The skin lesions erythema nodosum and pyoderma
gangrenosum are associated with UC and both normally resolve
with good colitis control.
• The eyes can be afected by uveitis and episcleritis.

12. ACUTE COLITIS
• Approximately 5% of patients present with acute severe (fulminant)
colitis.
• Intensive medical treatment leads to remission in 70% but the
remainder require urgent surgery.
• Toxic dilatation should be suspected when patients develop severe
abdominal pain and confirmed by the presence on a plain abdominal
radiograph of a colon with a diameter of more than 6 cm .
• A reduction in stool frequency is not always a sign of improvement in
patients with acute severe colitis, and a falling stool frequency,
abdominal distension and abdominal pain (resulting from
progression of the infammatory process through the colonic wall) are
strongly suggestive of fulminant colitis and impending perforation.

13. • Plain abdominal radiographs or abdominal computed
tomography (CT) may help monitor disease progression in
patients with acute severe colitis.
• Progressive increase in colon diameter despite medical
therapy is an indication for urgent surgery.
• Colonic perforation is a grave complication with a mortality
rate of 40%.
• Steroids may mask the physical signs.
• Severe haemorrhage is uncommon (1–2%) but may
occasionally require urgent surgical intervention.

14. CANCER RISK IN COLITIS
• The risk of cancer in ulcerative colitis increases with duration of disease.
• At 10 years from diagnosis, it is approximately 1%, increasing to 10–15% at 20
years and 20% at 30 years.
• Patients with pancolitis (defined as the presence of infammation proximal to
the splenic fexure) of more than 10 years’ duration should be entered into
endoscopic screening programmes in order to detect clinically silent
dysplasia, which is predictive of increased cancer risk.
• Malignant change, often atypical and high grade, may be multifocal or
submucosal.
• Colonoscopic surveillance with dye spray (chromoendoscopy) or multiple
biopsies every 10 cm should look for subtle mucosal abnormalities, which
can occur in fat mucosa or a DALM.
• Patients with UC and sclerosing cholangitis are also at a signifcantly greater
risk of development of large bowel cancer.

15. Resection specimen from a patient with longstanding ulcerative colitis
showing a narrow tubular colon with areas of cancerous change in the
rectum and sigmoid

17. INVESTIGATIONS
ENDOSCOPY AND BIOPSY
Rigid/fexible sigmoidoscopy can detect proctitis
the mucosa is1.hyperaemic, 2.bleeds on touch, 3.purulent exudate
In cases with remission and relapse 1.regenerative mucosal nodules or
2.pseudopolyps.
Colonoscopy with biopsy has a key to determine 1.the extent of infammation
2.to distinguish between UC and Crohn’s colitis to monitor the response to
treatment;
3.to assess longstanding cases for malignant change.
colonoscopy is contraindicated in severe acute colitis because of the risk of colonic
perforation
Endoscopic fndings can be combined with clinical features and the physician’s
assessment to produce a disease activity score known as Mayo score for

18. Radiology
• A plain abdominal film to demonstrate the development of toxic megacolon.
• Barium enema will show a featureless colon.
• CT findings in pancolitis may show significant thickening of the colonic wall,
inflammatory stranding in the colonic mesentery.
Bacteriology
• A stool specimen should be sent for microbiological analysis when UC is
suspected in order to exclude infective colitides, notably Campylobacter, which
may be very difcult to distinguish from acute severe UC.
• Clostridium diffcile colitis may need to be considered in populations at risk of this
disease).
• Cytomegalovirus infection is a major pathogen in immunocompromised patients
and can be diffcult to distinguish from UC.
• Superimposed infection may precipitate fulminant colitis.

19. MANAGEMENT OF UC
• multidisciplinary approach to management.
• include specialists in IBD gastroenterology, colorectal surgery, IBD nursing,
stoma therapy, gastrointestinal and interventional radiology, pathology, dieticians
and nutritional support services, clinical psychologist and other specialties
according to the individual patient’s need.

20. MEDICAL MANAGEMENT
• Conventional 1st line treatment is 5 Amino Salicylic Acid derivatives
• MOA : inhibitors of cyclo oxygenase
• Can be given topically or systemically
• Single agent 5ASA is used for treating 1. Ulcerative Proctitis
• 2. Maintenance therapy after induction of remission
• Corticosteroids form the mainstay of treatmentdue to their wide spread anti inflammatory action
• Can be given topically or systemically
• Azathioprine and ciclosporin immunosuppressive drugs to maintain remission and in maintenance therapy
as steroid sparing agents.
• Monoclonal antibodies Infliximab and adalimubab -TNF aplha antagonists
ustekinumab- interleukin 12/23 antagonist
• Vedolizumab and ertolizumab- Anti integrin mab
• Tofacitinib- JAK inhibitor
• Ozanimod- SIP receptor modulator

21. NUTRITIONAL SUPPORT
• It is essential that nutritional status is evaluated in all patients with
IBD.
• Patients with moderate nutritional impairment will require nutritional
supplementation
• Severely malnourished patients may require enteral tube or even
intravenous feeding.
• Anaemia, hypoproteinaemia and electrolyte, vitamin and metabolic
bone problems must be addressed.
• Nutritional optimisation has been shown to improve surgical
outcomes but it is important to recognise that a signifcant
improvement in nutritional status is very unlikely in the setting of active
infection; in patients with abscesses, efective drainage remains the
overwhelming priority.

22. ACUTE SEVERE COLITIS
Patients with a mild attack usually respond to a course of oral prednisolone.
A moderate attack often responds to oral prednisolone, twice-daily steroid enemas
and ASA.
Failure to achieve remission as an outpatient is an indication for admission.
Acute severe colitis occurs in up to 10% of patients, who require hospital
admission.
Regular assessment of vital signs, weight and the abdomen are required.
A stool chart should be kept, regular clinical review is required and supine
abdominal radiographs should be done when there is clinical concern for toxic
megacolon.
The presence of mucosal islands or intramural gas on plain radiographs, increasing
colonic diameter or a sudden increase in pulse and temperature may indicate
impending colonic perforation.
Limited endoscopic assessment and reassessment is useful in monitoring response

23. Initial treatment is with intravenous steroids. Regular and joint
review by a gastroenterologist and a colorectal surgeon is
essential to identify patients who are failing to make anticipated
progress and to ensure that surgery is neither inappropriately
delayed nor inappropriately undertaken. Patients should be
supported by IBD specialist nurses and early introduction to a
stoma therapist is considered best practice.
Instigation of immunosuppressive therapy with either intravenous
ciclosporin A or an anti-TNFα agent may be appropriate
however, surgery should be considered if rescue therapy does
not result in rapid clinical improvement for the patient.
Clinical deterioration requires urgent colectomy.

24. INDICATIONS FOR SURGERY
The overall lifetime risk of colectomy for a patient with UC is about 20%.
INDICATIONS
severe or fulminating disease failing to respond to medical therapy
chronic disease with anaemia, frequent stools, urgency and tenesmus
steroid-dependent disease where remission cannot be maintained
without substantial doses of steroids with harmful side effects.
intolerance or side efects of medical therapy required to control the
disease, e.g. steroid psychosis, azathioprineinduced pancreatitis;

25. • growth retardation in children or adolescents;
• neoplastic change: patients who have severe dysplasia or
carcinoma;
• associated sclerosing cholangitis;
• extraintestinal manifestations;
• rarely, severe haemorrhage or stenosis causing obstruction.

26. SURGICAL MANAGEMENT- EMERGENCY
Safest procedure for malnourished and pts on high dose steroids is
subtotal colectomy with end ileostomy
Rectosigmoid remnant can be brought out as a formal mucous
fistula or a subfascial closure can be done
Restorative surgery can be done once pt is completely improved
and is no longer on steroids.
Proctectomy is rarely needed in the emergency situation

27. Subfascial closure of the rectal remnant following subtotal colectomy
and end-ileostomy for acute ulcerative colitis (a). The rectal remnant
can alternatively be brought to the skin as a mucus fstula (b).

28. Surgical management- elective
1.subtotal colectomy and ileostomy (as in an urgent colectomy)
2.proctocolectomy and permanent end-ileostomy;
3.restorative proctocolectomy with ileal pouch–anal anastomosis
(IPAA);
4.subtotal colectomy and ileorectal anastomosis;
5.segmental colectomy (Crohn’s colitis only).

29. Three ways of forming a pouch are illustrated:
(a) a simple reversed ‘J’;
(b) an ‘S’ pouch;
(c) a ‘W’ pouch.

30. Stapled ‘J’ pouch with the stapler creating an ileal pouch– anal
anastomosis

31. INDETERMINATE COLITIS
• Approximately one in 10 patients with colitis presents with histological features
that make their disease difficult to characterize.
• While the clinical history may suggest the diagnosis in some cases (for example,
a history of recurrent perianal sepsis and fistulation would make a diagnosis of CD
more likely), in others it may remain unclear whether a patient has UC or CD.
• In such cases, it may still be appropriate to offer IPAA after detailed informed
consent, but the risks of pouch failure appear to be significantly higher (up to 25–
30%) and patients should be advised accordingly.

32. CROHNS DISEASE(REGIONAL COLITIS)
characterised by a chronic full-thickness infammatory process that can afect
any part of the gastrointestinal tract from the lips to the anal margin.
most common in North America and northern Europe, with an annual
incidence of 8 per 100 000.
CD is slightly more common in women and is most frequently diagnosed
between the ages of 25 and 40 years.
There is a second peak of incidence around the age of 70 years.
The incidence is rising in Asia, which is attributed to increased urbanisation.
There are differences in clinical manifestations in Asian populations, with a
higher male predominance, more perianal involvement, fewer extraintestinal
manifestations and worse clinical outcomes.

33. ETIOLOGY
complex interplay of genetic and environmental factors
similarity to Johne’s disease of cattle, a chronic infammatory
enteropathy resulting from infection with Mycobacterium
paratuberculosis
but trials have not demonstrated any therapeutic beneft of treating CD
with antituberculous drugs.
considerable recent interest in food additives, particularly
preservatives that may support a proinfammatory dysbiosis in the gut
microbiome.
An association with high levels of sanitation in childhood has also
been implicated.
Smoking increases the relative risk of CD threefold and is an

34. Approximately 10% of patients have a frst-degree relative with the disease, and
concordance approaches 50% in monozygotic twins.
Inheritance is thought to involve multiple genes with low penetrance.
Variants of NOD2/CARD15, a gene involved in intracellular recognition of
bacteria, have been shown to have a strong association with CD.
Most patients have no identifable germline mutational signature, and epigenetic
mutations are more likely to be involved.
Both UC and CD are associated with alterations in the gut microbiome, with
generally decreased microbial diversity.

35. PATHOGENESIS
• In both CD and UC increased gut mucosal permeability appears to develop at a
relatively early stage and may lead to increased passage of luminal antigens
that induce a cell-mediated inflammatory response.
• Proinflammatory cytokines, such as interleukin-2 and tumour necrosis factor,
are then released.
• It has been suggested that CD is associated with a defect in suppressor T cells.
• Animal studies have suggested that the increase in gut permeability develops
because of changes in bacterial recognition proteins and an increase in
inflammatory gene activation before macroscopic evidence of inflammation
develops.
• genetically determined increase in gut permeability, perhaps combined with an
abnormal immune-mediated response to colonization of the gut with enteric
microflora, may initiate the disease.

36. PATHOLOGY
The terminal ileum is the most commonly afected segment of bowel in patients with
CD.
More proximal small bowel is less frequently involved.
Colitis alone occurs in up to one-third of cases, the stomach and duodenum are
afected in around 5% of cases, but perianal lesions are common, affecting up to
50% of patients.
Perianal disease occurs in 25% of patients with small bowel disease and in 75% of
patients with Crohn’s colitis.
Macroscopically CD is characterised by fbrotic thickening of the intestinal wall with
narrowing (stricturing) of the lumen and fat wrapping (encroachment of mesenteric
fat around the bowel) .
There is usually dilated bowel just proximal to the stricture and deep mucosal
ulcerations with linear or serpiginous (snake-like) patterns in the strictured area
itself.

37. Oedema between ulcers gives rise to a characteristic cobblestone
appearance of the mucosa .
The trans-mural infammation (a pathognomonic feature of CD) may
lead to segments of bowel becoming adherent to each other and to
surrounding structures, forming infammatory masses with mesenteric
abscesses and fstulation into adjacent organs.
The serosa is usually opaque, with thickening of the mesentery and
enlarged mesenteric lymph nodes. CD is characteristically
discontinuous, with infamed areas separated by apparently normal
intestine, so-called skip lesions.

38. Microscopically focal areas of chronic infammation involving all
layers of the intestinal wall with lymphoid aggregates are
characteristic of CD.
Non-caseating giant cell granulomas found in 60% of patients
are pathognomonic of CD .
They are most commonly seen in anorectal disease.
Multifocal arterial occlusions are found in thickened muscularis
propria.
There may be nerve cell hyperplasia and deep, fssuring
ulceration within afected areas.
Characteristically, and unlike in UC, there may be completely
normal areas immediately next to areas of severe infammation.

39. Crohn’s disease of the ileocaecal region showing typical thickening of
the wall of the terminal ileum with encroachment of mesenteric fat.

40. Crohn’s disease of the terminal ileum illustrating longitudinal ulceration
and cobblestone mucosa.

41. Resected specimen of terminal ileum and sigmoid colon illustrating Crohn’s
disease of the terminal ileum with multiple enterocolic fstulae.

42. CLINICAL FEATURES
Occasionally, CD presents acutely with ileal inflammation and symptoms and signs
resembling those of acute appendicitis or, much less commonly, free perforation of
the small intestine resulting in a local or diffuse peritonitis.
CD may present with acute severe colitis but this is considerably less common
than in UC.
Small bowel CD often presents with bouts of abdominal pain and mild diarrhea.
A tender mass may be palpable in the right iliac fossa.
Intermittent fever, anemia and weight loss are common.
After months of repeated attacks characterized by acute inflammation, the affected
area of intestine stenoses with fibrosis, causing chronic obstructive symptoms.
Children developing the illness before puberty may have retarded growth and
sexual development.
As CD progresses, transmural fissuring, intra-abdominal abscesses and fistulae
may develop.

43. • Fistulation may occur into adjacent loops of bowel (enteroenteric or
interloop fistulae).
• Occasionally, a mobile loop of sigmoid loop may become adherent to
the affected terminal ileum, resulting in ileosigmoid fistulation .
• The fistula tracks in such cases are usually small and the profuse
diarrhoea that results from Ileo sigmoid fistulation is due primarily to
bacterial overgrowth (attributable to colonisation of the small bowel
with colonic fora) rather than passage of small bowel content into the
colon.
• Fistulation may also occur into the bladder (enterovesical), the female
genital tract or, less commonly, the duodenum. Fistulation to the
abdominal wall (enterocutaneous fistula) may also develop
spontaneously or following appendicectomy in unrecognised CD, but
more commonly presents as a complication of abdominal surgery.

44. COLONIC CROHNS DISEASE
Colonic involvement is found in 30% of patients with CD, frequently in association
with perianal disease, and may coexist with small bowel pathology.
Colonic CD presents with symptoms of colitis and proctitis as described for UC,
although toxic megacolon is much less common.
Colonic strictures may form just as are seen in small bowel CD. Endoscopic
dilatation may be performed as an alternative to surgical resection. The presence
of skip lesions, rectal sparing, non-caseating granulomas or perianal disease will
point to CD.
Many patients with CD present with perianal problems.The perianal skin can have
a bluish tinge. Large, oedematous and infamed skin tags are common. Fissures
and superfcial ulcers with undermined edges are relatively painless and can heal
with bridging of epithelium. Deep cavitating ulcers are usually found in the upper
anal canal; they can be painful and cause perianal abscesses and fstulae.
Fistulation through the posterior wall of the vagina may lead to rectovaginal fstula
and continuous leakage of gas and/or faeces per vagina.

45. • The rectal mucosa is often spared in CD and will feel normal on rectal
examination.
• If involved, it may feel thickened, nodular and irregular.So,Severe CD proctitis
may occasionally be mistaken for cancer.
• Perianal disease is frequently associated with dense, fbrous stricturing (stenosis)
at the anorectal junction.
• Incontinence may develop because of destruction of the anal sphincter
musculature owing to infammation, abscess formation, fbrosis and repeated
surgical drainage.
• In severe cases, the perineum may become densely fbrotic, rigid and covered
with multiple discharging openings (watering-can perineum).
• Each patient with CD should have their disease phenotype (manifestations)
classifed according to the Montreal classifcation. The Montreal classifcation
specifes age at diagnosis, behaviour and disease location.

47. EXTRA INTESTINAL MANIFESTATIONS
Primary sclerosing cholangitis is relatively rare in CD, compared with UC.
Gallstones are common, as an infamed or absent (because of resection) terminal
ileum leads to reduced absorption of bile salts.
Amyloidosis is common but is rarely symptomatic.
Metastatic CD can occur in the vagina and/or skin with nodular ulcers, which
demonstrate non-caseating granulomas when biopsied.
Such cutaneous CD can be virtually indistinguishable macroscopically from
hidradenitis suppurativa.